The nature of the immune response (Ir) gene defect for pigeon cytochrome c in [B10.A(4R) x B10.PL]F1 mice. A comparison between thymic selection and antigen presentation.
The nature of the immune response (Ir) gene defect for pigeon cytochrome c in [B10.A(4R) x B10.PL]F1 mice. A comparison between thymic selection and antigen presentation.
复制标题
[B10.A(4R) x B10.PL]F1 小鼠中鸽子细胞色素 c 的免疫反应 (Ir) 基因缺陷的性质。
作者：
Z. Kovač;R. Schwartz
[B10.A（4 R）x B10.PL]F1小鼠对鸽子细胞色素c有低应答，而[B10.A（2 R）x B10.PL]F1和B10.A小鼠对鸽子细胞色素c有高应答。通过建立两组不同的辐射诱导的骨髓嵌合体，研究了E α Ia分子的不同同种异型物对鸽子细胞色素c的免疫应答发挥其Ir基因效应的体内位点。[B10.A（4R）x B10.PL]F1（b.m.）- B10.A（irr.）嵌合体具有低应答者的抗原呈递细胞（APC），但其T细胞在高应答者环境中接受训练，被发现是对鸽子细胞色素c的低应答者。相比之下，B10.A（b.m.）- [B10.A（4R）x B10.PL]F1（irr.）嵌合体具有高应答型的APC，但其T细胞在低应答环境中接受训练，对鸽子细胞色素c有应答。在抗原引发之前和体外二次攻击时，向第一种类型的嵌合体中加入B10.A APC，将50%的动物转化为应答者。此外，[B10.A（4 R）x B10.PL]F1小鼠如果用10倍以上的抗原剂量致敏并在B10.A APC存在下进行体外再刺激，则对鸽子细胞色素c有反应。这些结果表明，在这个系统中的Ir基因缺陷的主要网站是在抗原呈递的水平，而不是在T细胞库。
[B10.A(4R) x B10.PL]F1 mice are low responders to pigeon cytochrome c, while [B10.A(2R) x B10.PL]F1 and B10.A mice are high responders. The in vivo site at which the different allomorphs of the E alpha Ia molecule exert their Ir gene effect on the immune response to pigeon cytochrome c was examined by creating two different sets of radiation-induced bone marrow chimeras. [B10.A(4R) x B10.PL]F1(b.m.)----B10.A(irr.) chimeras, which possess antigen-presenting cells (APC) of the low responder, but whose T cells are educated in a high responder environment, were found to be low responders to pigeon cytochrome c. In contrast, B10.A(b.m.)----[B10.A(4R) x B10.PL]F1(irr.) chimeras, which possess APC of the high responder type, but whose T cells are educated in a low responder environment, responded to pigeon cytochrome c. Addition of B10.A APC to the first type of chimera, both prior to antigen priming and at the time of the secondary challenge in vitro, converted 50% of the animals to responders. Furthermore, [B10.A(4R) x B10.PL]F1 mice responded to pigeon cytochrome c if they were primed with a 10-fold greater antigen dose and restimulated in vitro in the presence of B10.A APC. These results suggest that the primary site of the Ir gene defect in this system is at the level of antigen presentation and not in the T cell repertoire.